Evidence map›Paper›PMID 35149115›Full record

ReviewLife sciences2022

The therapeutic potential of regulatory T cells in reducing cardiovascular complications in patients with severe COVID-19.

Nafiseh Saghafi, Seyed Abdolrahim Rezaee, Amir Abbas Momtazi-Borojeni, Fataneh Tavasolian, Thozhukat Sathyapalan, Elham Abdollahi, Amirhossein Sahebkar

Open access · greenAbstract readReview
In one paragraph

Review in Life sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.9field-weighted citation impact, top 26% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed, 10 citations in OpenAlex.

  1. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 6 institutions in 4 countries.

Nafiseh SaghafiDepartment of Gynecology, Woman Health Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.
Seyed Abdolrahim RezaeeDepartment of Immunology and Allergy, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran; Research Center for HIV/AIDS, HTLV and Viral Hepatitis, Iranian Academic Center for Education, Culture and Research (ACECR), Mashhad Branch, Mashhad, Iran; Inflammation and Inflammatory Diseases Research Center, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Amir Abbas Momtazi-BorojeniDepartment of Medical Biotechnology and Nanotechnology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Fataneh TavasolianToronto Western Hospital, Toronto, Canada.
Thozhukat SathyapalanAcademic Diabetes, Endocrinology and Metabolism, Hull York Medical School, University of Hull, UK.
Elham AbdollahiDepartment of Gynecology, Woman Health Research Center, Mashhad University of Medical Sciences, Mashhad, Iran; Department of Immunology and Allergy, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. Electronic address: Abdollahie@mums.ac.ir.
Amirhossein SahebkarApplied Biomedical Research Center, Mashhad University of Medical Sciences, Mashhad, Iran; Biotechnology Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran; School of Medicine, The University of Western Australia, Perth, Australia; Department of Biotechnology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran. Electronic address: sahebkara@mums.ac.ir.
Mashhad University of Medical Sciences · IRAcademic Center for Education, Culture and Research · IRAlborz University of Medical SciencesToronto Western Hospital · CAUniversity of Hull · GBUniversity of Western Australia · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The SARS coronavirus 2 (SARS CoV-2) causes Coronavirus Disease (COVID-19), is an emerging viral infection. SARS CoV-2 infects target cells by attaching to Angiotensin-Converting Enzyme (ACE2). SARS CoV-2 could cause cardiac damage in patients with severe COVID-19, as ACE2 is expressed in cardiac cells, including cardiomyocytes, pericytes, and fibroblasts, and coronavirus could directly infect these cells. Cardiovascular disorders are the most frequent comorbidity found in COVID-19 patients. Immune cells such as monocytes, macrophages, and T cells may produce inflammatory cytokines and chemokines that contribute to COVID-19 pathogenesis if their functions are uncontrolled. This causes a cytokine storm in COVID-19 patients, which has been associated with cardiac damage. Tregs are a subset of immune cells that regulate immune and inflammatory responses. Tregs suppress inflammation and improve cardiovascular function through a variety of mechanisms. This is an exciting research area to explore the cellular, molecular, and immunological mechanisms related to reducing risks of cardiovascular complications in severe COVID-19. This review evaluated whether Tregs can affect COVID-19-related cardiovascular complications, as well as the mechanisms through which Tregs act.

Indexed as

SARS-CoV-2Adoptive TransferAnimalsCardiovascular DiseasesCOVID-19Cytokine Release SyndromeHumansInflammationT-Lymphocytes, RegulatoryCardiovascular complicationsCOVID-19SARS CoV-2TreatmentTregs

Identifiers

PMID35149115
PMCPMC8824166
OpenAlexW4210846678

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.